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Advanced Cell Biology > Lecture 16 - Apoptosis > Flashcards

Lecture 16 - Apoptosis Flashcards

1
Q

Three types of cell death

A
  1. Necrosis (exploding)
  2. Programmed cell death (suicide)
  3. Autophagy (organelle cannibalism)
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2
Q

Necrosis is induced by

A

Insults to the cell that cannot be repaired:

Injury, infection, cancer, infarction

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3
Q

Steps of necrosis (4)

A
  1. Cells swell, organelle membranes break down and chromatin is digested
  2. Cells lyse and spill contents into surrounding area
  3. Hydrolytic enzymes from lysosomes damage other nearby cells
  4. Leads to inflammation and self perpetuating gangrene
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4
Q

Apoptosis is used

A

In the developing nervous system, developing foetus, tadpole frog development, quality control, t and b cells

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5
Q

In the developing nervous system, apoptosis is used

A

To reinforce correct neuron connections

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6
Q

In the developing foetus, apoptosis is used

A

To form individual digits (from webbing)

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7
Q

In the tadpole, apoptosis is used

A

To form legs - cells in the tail die, governed by thyroid hormone

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8
Q

Apoptosis is also used as a

A

Quality control - abnormal, non functional or misplaced cells are removed, balance

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9
Q

Apoptosis and the immune system

A

T and B cells are trained to apoptose foreign antigens

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10
Q

Apoptosis and balance

A

Surplus cells eliminated

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11
Q

Steps of apoptosis ‘falling leaves’ (silent) (8)

A
  1. Cells shrink
  2. Cytoskeleton collapses
  3. Golgi fragments
  4. NE disassembles
  5. Chromatin hyper condenses and is digested
  6. Blebbing of the membrane and apoptotic bodies
  7. Alteration of the cell membrane so it is recognised by macrophages
  8. Membrane becomes permeable to small molecules
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12
Q

How is apoptosis mediated?

A

Specific class of proteases - Cys residue in active site, cleave at Asp

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13
Q

Caspases (C-Asp-ases)

A

Proteases in apoptosis

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14
Q

Procaspases (inactive caspases) are activated by

A

Cleavage

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15
Q

Procaspase cleavage sites are

A

Asp residues themselves

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16
Q

When the Procaspase is cleaved

A

The cleaved units reassociate to form a heterotetrameric Caspase with large and small subunits

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17
Q

Procaspases are

A

Hetero dimers

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18
Q

Caspases are

A

Hetero tetramers

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19
Q

Procaspase cleavage is mediated by

A

Initiator caspases (Upstream)

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20
Q

The caspase cascade

A

Amplifies the initial signal

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21
Q

The initiator caspase

A

Starts the cascade

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22
Q

The executioner caspases

A

Amplify the signal

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23
Q

What do caspases cleave? (at asp)

A
  1. Nuclear lamin

2. Cytosolic protein

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24
Q

Caspase activity is highly regulated because

A

Unregulated apoptosis could have catastrophic effects for the organism

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25
Q

The caspase cascade is

A

Irreversible

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26
Q

Two ways of activating apoptosis

A
  1. Extrinsic cascade

2. Intrinsic cascade

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27
Q

The Extrinisic cascade contains certain extracellular signalling proteins

A

TNF (death signal), Fas (death receptor)

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28
Q

The death domain

A

Transmembrane domain where TNF binds to Fas to signal apoptosis

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29
Q

Binding of TNF to Fas causes

A

Clustering of death domains (multimers) in the PM

Activates apoptosis

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30
Q

Caspases associate with the death domain to

A

Activate the caspase cascade

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31
Q

Clustering of the death domains is known as

A

Lipid raft fusion

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32
Q

The death domains are activated by

A

Conformational change

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33
Q

The death domain recruits the

A

DISC

Death inducing signalling complex

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34
Q

Proteins in the DISC

A

FADD, TRADD, Caspase 8/10

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35
Q

Example of the Extrinsic cascade (4)

A

Viral infection
1. viral proteins are cleaved and displayed on the surface of cells

  1. T killer cells recognise foreign peptide on Fas receptor
  2. Fas ligand on T killer cell binds to the Fas receptor
  3. Activates the death domain and caspase cascade
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36
Q

The Intrinsic Pathway involves

A

Mitochondria

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37
Q

The intrinsic pathway is triggered by

A

Injury (DNA damage, hypoxia)

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38
Q

Initial activators of the intrinsic pathway

A

Are not known

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39
Q

Activation of the apoptotic pathway leads to activation of

A

Bcl proteins

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40
Q

Bcl proteins are either

A

Pro apoptotic or anti apoptotic

41
Q

Bcl proteins form

A

Heterodimers in the cytoplasm

42
Q

In the absence of an intrinsic apoptotic signal, Bcl2 proteins

A

Bind to and inhibit BH123 proteins (pro apoptotic proteins)

43
Q

BH123

A

Pro apoptotic protein found on the outer mitochondrial membrane

44
Q

BH3 proteins

A

Pro apoptotic protein that binds Bcl2

45
Q

In the presence of a signal, BH3

A

Are activated and bind Bcl2

46
Q

Once the Bcl2 protein is bound by BH3,

A

BH123 becomes active and aggregates, and the mitochondria release cytochrome c

47
Q

What protein is released by the mitochondria that induces apoptosis?

A

Cytochrome C

48
Q

What protein does Cytochrome c bind to?

A

Apaf1

Apoptotic protease activating factor

49
Q

When Cyt c binds to Apaf1

A

A domain on Apaf is exposed which allows oligomerisation of Apaf into the Apoptosome

50
Q

The Apoptosome structure

A

Oligomer of 7 Apaf1 proteins with bound Cyt c

Plus a central procaspase9

51
Q

The procaspase9 in the apoptosome is the

A

Initiator caspase (activates the executioner caspases)

52
Q

IAPs

A

Inhibitors of apoptosis

53
Q

IAPs were originally discovered in

A 
Insect viruses (baculoviruses)
Also present in most animal cells
54
Q

IAPs have a

A

BIR domain

55
Q

The BIR domain in IAPs binds

56
Q

Anti IAPs

A

Block the IAPs

Located in the mitochondria

57
Q

To avoid apoptosis, most animal cells require

A

Continuous signalling from neighbouring cells

58
Q

Survival factors bind

A

To cell surface receptors

59
Q

How do survival factors suppress apoptosis (3)

A
  1. Stimulating transcription of Bcl2 proteins (anti apop)
  2. Phosphorylation (by Akt) of apoptotic proteins
  3. Phosphorylation (MAPK pathway) of anti IAPs
60
Q

If a cell is deprived of growth signals, what protein is activated

A

Jnk

Stress activated MAP kinase

61
Q

Jnk leads to the transcription of

A

BIM

Activates the intrinsic pathway

62
Q

Anoikis is the

A

State of being without a home

Cell adhesion dependent apoptosis

63
Q

If cells detach from the ECM

A

They must be destroyed

64
Q

Why do cells die if they detach from the tissue and the ECM?

A

Survival signals are mediated through cell-cell contacts (integrins)
Without these intrinsic apoptosis is triggered

65
Q

How is the survive signal mediated?

A

Directly - FAK and ILK (non receptor Tyr Kinases) maintain intracellular pathways

Indirectly - Integrins cause clustering of cell survival receptors in the PM

66
Q

Akt phosphorylates and inactivates

A

Bad and caspase9

67
Q

PI3K phosphorylates and inactivates

A

Bim, leads to its degradation

68
Q

If a cell loses interaction of integrins and ECM

A

Akt and PI3K pathways are deactivated

Apoptosis triggered

69
Q

When the Akt and PI3K pathways are deactivated

A

Caspase9 and BH3 proteins are activated

Apoptosis triggered

70
Q

The apoptotic extrinsic and intrinsic pathways are

71
Q

In some cells the intrinsic pathway is recruited by the extrinsic pathway to

A

Amplify the signalling cascade

72
Q

Caspase8 cleaves

A

BH3 protein BID into tBID

tBID binds and inhibits Bcl2

73
Q

tBID inhibits

74
Q

Bid, Bim and Puma

A

All inihibit Bcl2
Potent activators of apoptosis
Link between cell stimuli and apoptosis

75
Q

Apoptotic blebbing of membrane requires assembly of

A

Conical actin ring that undergoes MyosinII dependent contraction

76
Q

ROCK is a

A

Rho kinase that forms the conical actin ring for blebbing

when cleaved by caspase

77
Q

IF and MTs are cleaved by

78
Q

Dismantling and remodelling by caspases allows

A

Packaging of material into apoptotic bodies

79
Q

The apoptotic bodies are engulfed by

A

Phagocytes

80
Q

Apoptosis also triggers

A

Ca2+ release which increases apop events

81
Q

The ER loses it’s tubulo-reticular shape and forms

A

Cortical sheets and vesicles

82
Q

The Golgi fragments when

A

Caspases cleave Golgins

Cleaved Golgins further trigger apoptosis

83
Q

Cleaved Golgins

A

Translocate to mitochondria (GRASP65) or nucleus (GM130)

84
Q

Apoptotic cells fail to maintain

A

The polarity of phosphatidylserine

exposes inside to outside

85
Q

Cleavage of Lamin B by caspases allows

A

Larger than normal proteins into the nucleus to fragment DNA

86
Q

DFF

A

DNA fragmentation factor
Cleaves DNA between nucleosomes
Inactive heterodimer except during apoptosis

87
Q

DFF is activated by

88
Q

During autophagy, what sequesters cytosol and proteins?

A

Phagophores containing TM Atg proteins

89
Q

Phagophores fuse to form

A

Autophagosomes

90
Q

What protein allows the autophagosome to fuse with the lysosome?

A

LC3 protein

91
Q

Acid proteases are contained in the

92
Q

Excessive and insufficient apoptosis can both

A

Cause disease

93
Q

Neurodegeneration and Alzheimers disease is an example of

A

Excessive apoptosis (accumulation of aggregated insoluble protein fibres)

94
Q

Cancer is an example of

A

Insufficient apoptosis and autophagy

95
Q

An accumulation of faulty proteins (through a lack of autophagy) may trigger

96
Q

Bcl2 protein is a common

A

Lymphocyte cancer in humans

Over production of Bcl2 inhibits apoptosis

97
Q

Tumour suppressor P53 normally promotes

A

Apoptosis of DNA damaged cells

98
Q

Loss of P53 causes

A

Loss of apoptosis and cancer cell multiplication

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